Role of relaxin in regulation of fibrosis in the lung: Implications for airway remodeling in asthma

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8 Citations (Scopus)

Abstract

Airway remodeling changes are a key pathological feature of asthma. They are associated with airway hyperresponsiveness and fixed airway obstruction. Aged, relaxin-deficient mice display structural changes resembling airway remodeling in asthma, including thickening of the bronchial epithelium and extracellular matrix (ECM) deposition in the subepithelial region. Relaxin-deficient mice also have exaggerated airway remodeling in models of allergic airway disease compared to wild-type controls. Both in vitro and in vivo studies have suggested that airway fibrosis may drive other changes of airway remodeling, including epithelial changes. A suggested paradigm is that subepithelial fibrosis (deposition of ECM in the basement membrane region) may lead to increased epithelial cell proliferation and transforming growth factor-beta1 production, which in turn may lead to further fibrosis. Relaxin may therefore prevent or reverse activation of the epithelial and fibroblast remodeling in asthma. Control of epithelial remodeling and ECM production in the airway wall may play an important role in maintaining normal lung function. Understanding how relaxin protects against airway remodeling changes may have important implications in developing new therapies to treat airway remodeling in asthma.
Original languageEnglish
Pages (from-to)342 - 347
Number of pages6
JournalAnnals of the New York Academy of Sciences
Volume1160
DOIs
Publication statusPublished - 2009
Externally publishedYes

Cite this

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title = "Role of relaxin in regulation of fibrosis in the lung: Implications for airway remodeling in asthma",
abstract = "Airway remodeling changes are a key pathological feature of asthma. They are associated with airway hyperresponsiveness and fixed airway obstruction. Aged, relaxin-deficient mice display structural changes resembling airway remodeling in asthma, including thickening of the bronchial epithelium and extracellular matrix (ECM) deposition in the subepithelial region. Relaxin-deficient mice also have exaggerated airway remodeling in models of allergic airway disease compared to wild-type controls. Both in vitro and in vivo studies have suggested that airway fibrosis may drive other changes of airway remodeling, including epithelial changes. A suggested paradigm is that subepithelial fibrosis (deposition of ECM in the basement membrane region) may lead to increased epithelial cell proliferation and transforming growth factor-beta1 production, which in turn may lead to further fibrosis. Relaxin may therefore prevent or reverse activation of the epithelial and fibroblast remodeling in asthma. Control of epithelial remodeling and ECM production in the airway wall may play an important role in maintaining normal lung function. Understanding how relaxin protects against airway remodeling changes may have important implications in developing new therapies to treat airway remodeling in asthma.",
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Role of relaxin in regulation of fibrosis in the lung: Implications for airway remodeling in asthma. / Tang, Mimi; Samuel, Chrishan; Royce, Simon.

In: Annals of the New York Academy of Sciences, Vol. 1160, 2009, p. 342 - 347.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Role of relaxin in regulation of fibrosis in the lung: Implications for airway remodeling in asthma

AU - Tang, Mimi

AU - Samuel, Chrishan

AU - Royce, Simon

PY - 2009

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N2 - Airway remodeling changes are a key pathological feature of asthma. They are associated with airway hyperresponsiveness and fixed airway obstruction. Aged, relaxin-deficient mice display structural changes resembling airway remodeling in asthma, including thickening of the bronchial epithelium and extracellular matrix (ECM) deposition in the subepithelial region. Relaxin-deficient mice also have exaggerated airway remodeling in models of allergic airway disease compared to wild-type controls. Both in vitro and in vivo studies have suggested that airway fibrosis may drive other changes of airway remodeling, including epithelial changes. A suggested paradigm is that subepithelial fibrosis (deposition of ECM in the basement membrane region) may lead to increased epithelial cell proliferation and transforming growth factor-beta1 production, which in turn may lead to further fibrosis. Relaxin may therefore prevent or reverse activation of the epithelial and fibroblast remodeling in asthma. Control of epithelial remodeling and ECM production in the airway wall may play an important role in maintaining normal lung function. Understanding how relaxin protects against airway remodeling changes may have important implications in developing new therapies to treat airway remodeling in asthma.

AB - Airway remodeling changes are a key pathological feature of asthma. They are associated with airway hyperresponsiveness and fixed airway obstruction. Aged, relaxin-deficient mice display structural changes resembling airway remodeling in asthma, including thickening of the bronchial epithelium and extracellular matrix (ECM) deposition in the subepithelial region. Relaxin-deficient mice also have exaggerated airway remodeling in models of allergic airway disease compared to wild-type controls. Both in vitro and in vivo studies have suggested that airway fibrosis may drive other changes of airway remodeling, including epithelial changes. A suggested paradigm is that subepithelial fibrosis (deposition of ECM in the basement membrane region) may lead to increased epithelial cell proliferation and transforming growth factor-beta1 production, which in turn may lead to further fibrosis. Relaxin may therefore prevent or reverse activation of the epithelial and fibroblast remodeling in asthma. Control of epithelial remodeling and ECM production in the airway wall may play an important role in maintaining normal lung function. Understanding how relaxin protects against airway remodeling changes may have important implications in developing new therapies to treat airway remodeling in asthma.

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